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genetic and environmental influences on depression and anxiety

Inclusion of Specific Environmental and Endophenotypic Variables in Behavior Genetic Models Standard behavior genetic analyses represent genetic and environmental influences as unspecif ied, anonymous, or ‘‘black box’’ variables. Kendler notes that the statistical power to detect shared environmental influences is low in such standard models, whereas incorporating specified environmental variables within a behavior genetic model increases the power to detect such influences if they are present.

Accordingly, behavior genetic research has begun to incorporate specific environmental measures to detect the effects of these variables against a background of multiple genetic and environmental influences. Perhaps the most widely cited example of this approach is one that is relevant to the etiology of depression and anxiety disorders in adults. The results of standard behavior genetic analyses of twin data, reviewed earlier, typically have not suggested any significant role for shared environmental influences in the etiology of adults’ mood and anxiety disorder symptoms. Kendler, Neale, Kessler, Heath, and Eaves demonstrated a statistically significant effect of childhood parental loss (i.e., separation or death) on liability to DSMIII-R major depression, GAD, phobias, and panic disorder in adult females, against a background of other (anonymous) genetic and environmental risk factors.

Nonetheless, the estimated relative magnitude of this influence in explaining variation in liability to mood and anxiety disorders in adulthood was small (accounting for 4.9% of the variance in liability to panic disorder, 2.9% of the variance in liability to phobias, 2.5% of the variance in liability to GAD, and 1.6% of the variance in liability to major depression in the population of women studied).

Thus, this study represents a specific example of a more general research design, namely, including specific, putative causal mechanisms within multivariate behavior genetic models. This extended behavior genetic design is appropriate for including many different types of putative causal variables (e.g., perinatal birth complications, measures of executive functions, psychopathological measures, specific family and/or neighborhood environmental variables) within behavior genetic models. Findings from these studies can establish whether the relationship of such putative causal variables to the disorder is due primarily to common genetic or common environmental influences. These analyses can be useful for testing whether these putative causal variables represent endophenotypes that may be closer to the underlying genetic and environmental influences than the disorders themselves. Thus, another way to view such analyses is that they can help elaborate the specific causal mechanisms for a disorder that are captured by the broad and abstract genetic and environmental variance components that emerge from behavior genetic analyses. Another putative causal mechanism that may be included in behavior genetic models is specific candidate genes that are hypothesized to play some causal role in a disorder. With this in mind, we briefly discuss burgeoning molecular genetic studies of psychopathology in the next section.

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